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Induction of somatic hypermutation in immunoglobulin genes is dependent on DNA polymerase iota

Author

Listed:
  • Ahmad Faili

    (INSERM U373, Faculté de Médecine Necker-Enfants Malades)

  • Said Aoufouchi

    (INSERM U373, Faculté de Médecine Necker-Enfants Malades)

  • Eric Flatter

    (INSERM U373, Faculté de Médecine Necker-Enfants Malades)

  • Quentin Guéranger

    (INSERM U373, Faculté de Médecine Necker-Enfants Malades)

  • Claude-Agnès Reynaud

    (INSERM U373, Faculté de Médecine Necker-Enfants Malades)

  • Jean-Claude Weill

    (INSERM U373, Faculté de Médecine Necker-Enfants Malades)

Abstract

Somatic hypermutation of immunoglobulin genes is a unique, targeted, adaptive process. While B cells are engaged in germinal centres in T-dependent responses, single base substitutions are introduced in the expressed V h/V l genes to allow the selection of mutants with a higher affinity for the immunizing antigen. Almost every possible DNA transaction has been proposed to explain this process, but each of these models includes an error-prone DNA synthesis step that introduces the mutations1,2. The Y family of DNA polymerases3—pol η, pol ι, pol κ and rev1—are specialized for copying DNA lesions and have high rates of error when copying a normal DNA template4,5. By performing gene inactivation in a Burkitt's lymphoma cell line inducible for hypermutation, we show here that somatic hypermutation is dependent on DNA polymerase iota.

Suggested Citation

  • Ahmad Faili & Said Aoufouchi & Eric Flatter & Quentin Guéranger & Claude-Agnès Reynaud & Jean-Claude Weill, 2002. "Induction of somatic hypermutation in immunoglobulin genes is dependent on DNA polymerase iota," Nature, Nature, vol. 419(6910), pages 944-947, October.
    • Handle: RePEc:nat:nature:v:419:y:2002:i:6910:d:10.1038_nature01117
    DOI: 10.1038/nature01117
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